Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

Article Title: Adipokine Profile in Patients with Type 2 Diabetes Depends on Degree of Obesity

doi: 10.12659/MSM.904318

Figure Lengend Snippet: Leptin/adiponectin ratio in control group and type 2 diabetic patients divided according to BMI value. K – control group, group I – type 2 diabetic patients with normal body weight, group II – type 2 diabetic patients with overweight, group III – type 2 diabetic patients with obesity and group IV – type 2 diabetic patients with severe obesity. * p<0.05 vs. group K; ** p<0.01 vs. group K; # p<0.05 vs. group I.

Article Snippet: The plasma concentrations of the studied adipokines were determined by immunoenzymatic methods using Human Leptin Quantikine ELISA Kit (R&D Systems, USA), Human Total Adiponectin/Acrp30 Quantikine ELISA (R&D Systems, USA), and Human Resistin Quantikine ELISA Kit (R&D Systems, USA), as well as Human Nicotinamide phosphoribosyltransferase, NAmPRTase ELISA Kit (Wuhan EIAab Science, China) for leptin, adiponectin, resistin, and visfatin, respectively.

Techniques: Control

Journal: Food & Nutrition Research

Article Title: Cudrania tricuspidata water extract improved obesity-induced hepatic insulin resistance in db/db mice by suppressing ER stress and inflammation

doi: 10.3402/fnr.v59.29165

Figure Lengend Snippet: Levels of glucose, insulin, glucagon, and leptin in the C57BL/6J- db/db mice with dietary supplementation of Cudrania tricuspidata water extract

Article Snippet: Serum insulin, glucagon, and leptin were respectively measured with an Ultra Sensitive Mouse Insulin ELISA kit (Crystal Chem, Downers Grove, IL, USA), Glucagon Quantikine ELISA kit (R&D Systems, Minneapolis, MN, USA), and Mouse/Rat Leptin Quantikine ELISA kit (R&D Systems) according to the manufacturer's protocols.

Techniques: Control

Journal: Cell Death & Disease

Article Title: Marrow leptin-LEPR signaling rewires mitochondrial oxidative metabolism to confer chemoresistance in acute myeloid leukemia

doi: 10.1038/s41419-026-08528-0

Figure Lengend Snippet: A Schematic diagram of clinical significance analysis for bone marrow (BM) plasma leptin levels and blast-cell LEPR expression in 84 newly diagnosed AML patients. B BM plasma leptin levels correlate inversely with blast clearance rates in AML patients. C Leptin concentrations in BM plasma from AML patients with differential chemotherapeutic responses. D ROC curve of leptin in BM plasma for distinguishing ORR and NR groups. E Leptin levels in the BM plasma of AML patients stratified by ELN 2022 risk classification. F ROC curve of marrow plasma leptin for distinguishing between favorable and adverse risk AML groups. G ROC curve of marrow plasma leptin for distinguishing between intermediate and adverse risk AML groups. H CCK-8 analysis of cell viability in leptin-pretreated primary AML cells following 24 h Ara-C exposure ( n = 5). I The forest plot shows the results of logistic regression analysis. J Representative FCM profiles and MFI statistical analysis of LEPR expression in BM leukemia cells from high- and low-leptin groups ( n = 10 patients per group). MFI: mean fluorescence intensity. K Kaplan-Meier analysis of overall survival in AML patients stratified by LEPR expression levels from GSE1159 , GSE37642 and GSE6891 datasets. Data are presented as mean ± SD C, E, J . Significance differences were determined by two-tailed unpaired t test with Welch’s correction C , one-way ANOVA with Holm-Šídák’s multiple comparisons test (E), two-tailed paired t test H , or two-tailed unpaired t test J . ns, not significant, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Marrow plasma leptin concentrations were measured using a Human Leptin ELISA Kit (Cusabio, Wuhan, Hubei, China), with Spearman’s correlation ( r ) analyzing leptin-blast clearance relationships and comparative analyses examining leptin levels between ORR and NR groups.

Techniques: Clinical Proteomics, Expressing, CCK-8 Assay, Fluorescence, Two Tailed Test

Journal: Cell Death & Disease

Article Title: Marrow leptin-LEPR signaling rewires mitochondrial oxidative metabolism to confer chemoresistance in acute myeloid leukemia

doi: 10.1038/s41419-026-08528-0

Figure Lengend Snippet: A Experimental design of evaluating the role of leptin on the therapeutic effect in MLL-AF9-driven AML mice. B Kaplan-Meier survival curve of MLL-AF9 AML mice ( n = 5 mice per group). C Representative images and weight comparisons of spleen and liver in MLL-AF9 AML mice treated with PBS, Ara-C, leptin + Ara-C, or Allo-aca+ Ara-C ( n = 5 mice per group). D Representative H&E-stained sections of BM, spleen and liver (scale bars: 20 μm). E Representative FCM profiles (left) and quantification of YFP + AML cells in BM, spleen, and liver of MLL-AF9 AML mice ( n = 5 mice per group). Data are presented as mean ± SD C, E . Significance differences were determined by log-rank test B , or one-way ANOVA with Dunnett’s multiple comparisons test C, E . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Marrow plasma leptin concentrations were measured using a Human Leptin ELISA Kit (Cusabio, Wuhan, Hubei, China), with Spearman’s correlation ( r ) analyzing leptin-blast clearance relationships and comparative analyses examining leptin levels between ORR and NR groups.

Techniques: Staining

Journal: Cell Death & Disease

Article Title: Marrow leptin-LEPR signaling rewires mitochondrial oxidative metabolism to confer chemoresistance in acute myeloid leukemia

doi: 10.1038/s41419-026-08528-0

Figure Lengend Snippet: A Total antioxidant capacity analysis of blast-cell from MLL-AF9 (left) and AML1-ETO9a (right) AML mice ( n = 5 mice per group). B Effect of leptin on chemosensitivity to Ara-C and DNR in human AML cell lines (U937, HL-60, and THP-1). The inhibition rates were calculated from four treatment arms: (i) PBS control; (ii) Leptin alone; (iii) Ara-C alone (or DNR) and (iv) Leptin + Ara-C (or DNR). Data represent three independent biological experiments. C Analysis of total antioxidant capacity in leptin-treated AML cells. D GSH/GSSG ratio was examined with a GSH and GSSG assay kit. E RT-qPCR analysis of antioxidant-associated genes mRNA levels in leptin-treated AML cells. Analysis of CAT F and SOD G activity. H Representative immunofluorescence images (left) and MFI quantification (right) of LEPR expression (LEPR, green) in leptin-treated AML cells (scale bars: 25 μm). Data are presented as mean ± SD. Significance differences were determined by one-way ANOVA with Dunnett’s multiple comparisons test A , or two-tailed unpaired t test B–H . ns, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Marrow plasma leptin concentrations were measured using a Human Leptin ELISA Kit (Cusabio, Wuhan, Hubei, China), with Spearman’s correlation ( r ) analyzing leptin-blast clearance relationships and comparative analyses examining leptin levels between ORR and NR groups.

Techniques: Inhibition, Control, GSSG Assay, Quantitative RT-PCR, Activity Assay, Immunofluorescence, Expressing, Two Tailed Test

Journal: Cell Death & Disease

Article Title: Marrow leptin-LEPR signaling rewires mitochondrial oxidative metabolism to confer chemoresistance in acute myeloid leukemia

doi: 10.1038/s41419-026-08528-0

Figure Lengend Snippet: A Western blot analysis of LEPR expression in AML cells under indicated treatments. β-actin served as the loading control. Band intensities were quantified using ImageJ software and normalized to the control group. B–D Effect of Allo-aca on AML cell chemosensitivity by CCK-8 assay. The inhibition rates were calculated from eight treatment arms: (i) PBS; (ii) Allo-aca alone; (iii) Leptin alone; (iv) Allo-aca + Leptin; (v) Ara-C alone (or DNR); (vi) Allo-aca + Ara-C (or DNR); (vii) Leptin + Ara-C (or DNR) and (viii) Allo-aca + Leptin + Ara-C (or DNR). Data represent three independent biological replicates. E Western blot to confirm the depletion of LEPR in AML cells. β-actin served as a loading control. F Chemosensitivity analysis of LEPR -knockout AML cells with or without leptin treatment. Comparison of total antioxidant capacity G , GSH/GSSG ratio H , antioxidant-related genes mRNA levels I , CAT J and SOD K activity in AML cells with or without LEPR knockout. Data are presented as mean ± SD B–D, F–K . Significance differences were determined by two-tailed unpaired t test. ns, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Marrow plasma leptin concentrations were measured using a Human Leptin ELISA Kit (Cusabio, Wuhan, Hubei, China), with Spearman’s correlation ( r ) analyzing leptin-blast clearance relationships and comparative analyses examining leptin levels between ORR and NR groups.

Techniques: Western Blot, Expressing, Control, Software, CCK-8 Assay, Inhibition, Knock-Out, Comparison, Activity Assay, Two Tailed Test

Journal: Cell Death & Disease

Article Title: Marrow leptin-LEPR signaling rewires mitochondrial oxidative metabolism to confer chemoresistance in acute myeloid leukemia

doi: 10.1038/s41419-026-08528-0

Figure Lengend Snippet: A Numbers of DEPs located in mitochondria of MLL-AF9 leukemia cells ( n = 3 mice per group). B Venn diagram showing the overlapping DEPs that up-regulated in the leptin + Ara-C group but down-regulated in the Allo-aca + Ara-C group (versus Ara-C alone, n = 3 mice per group). C KEGG pathway enrichment analysis of B . D Heatmap analysis of OXPHOS (Ko00190) and ROS (Ko05208) pathway protein expression in MLL-AF9 leukemia cells. E Mitochondrial respiration analysis of sorted MLL-AF9 AML cells using Seahorse XF technology ( n = 5 mice per group). F Calculation of basal respiration (Basal), maximal respiratory capacity (Max), spare respiratory capacity (Spare), and mitochondrial ATP production (ATP) in MLL-AF9 leukemia cells based on the measurements in E . G Representative FCM profiles (left) and MFI quantification (right) of mtROS levels in MLL-AF9 leukemia cells by MitoSOX staining ( n = 5 mice per group). H Measurement of OCR levels in AML1-ETO9a leukemia cells. I Calculation of Basal, Max, Spare, and ATP in AML1-ETO9a leukemia cells based on the measurements in H . J Representative FCM profiles (left) and MFI statistical analysis (right) of mtROS levels in AML1-ETO9a leukemia cells. K OCR was measured (upper) and calculation of basal, Max, Spare, and ATP (lower) in leptin-treated AML cells. L Representative FCM histogram (upper) and MFI statistical analysis (lower) of mtROS levels in leptin-treated AML cells. Data are presented as mean ± SD F, G, I–L . Significance differences were determined by one-way ANOVA with Dunnett’s multiple comparisons test F, G, I, J , or two-tailed unpaired t test K, L . ns, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Marrow plasma leptin concentrations were measured using a Human Leptin ELISA Kit (Cusabio, Wuhan, Hubei, China), with Spearman’s correlation ( r ) analyzing leptin-blast clearance relationships and comparative analyses examining leptin levels between ORR and NR groups.

Techniques: Expressing, Staining, Two Tailed Test

Journal: Cell Death & Disease

Article Title: Marrow leptin-LEPR signaling rewires mitochondrial oxidative metabolism to confer chemoresistance in acute myeloid leukemia

doi: 10.1038/s41419-026-08528-0

Figure Lengend Snippet: A Gene Ontology (GO) terms enrichment analysis of up-regulated DEPs in the leptin + Ara-C group (upper) and down-regulated DEPs in the Allo-aca + Ara-C group (lower). B Heatmap analysis of mitochondrial complex I structural subunit protein expression in MLL-AF9 leukemia cells. C Structural model of mitochondrial respiratory chain complexes. D Comparison of complex I activity in AML cells treated with leptin, Allo-aca, or a combination. E Western blot analysis of p-STAT3 (727), p-STAT3 (705), STAT3, p-JAK2 (Tyr1007/1008) and JAK2 expression in AML cells under indicated treatments. β-actin served as a loading control. Rescue experiments of complex I activity F , total antioxidant capacity G and mtROS production H in AML cells. I CCK-8 analysis of the chemosensitivity in AML cells treated with leptin, JSI-124 (JAK2/STAT3 inhibitor), or leptin + JSI-124. Data are presented as mean ± SD D, F–I . Significance differences were determined by two-tailed unpaired t test D, I , or one-way ANOVA with Dunnett’s multiple comparisons test F–H . ns, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Marrow plasma leptin concentrations were measured using a Human Leptin ELISA Kit (Cusabio, Wuhan, Hubei, China), with Spearman’s correlation ( r ) analyzing leptin-blast clearance relationships and comparative analyses examining leptin levels between ORR and NR groups.

Techniques: Expressing, Comparison, Activity Assay, Western Blot, Control, CCK-8 Assay, Two Tailed Test